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2015 ; 12
(7
): 383-91
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Targeting glycogen metabolism in bladder cancer
#MMPMID26032551
Ritterson Lew C
; Guin S
; Theodorescu D
Nat Rev Urol
2015[Jul]; 12
(7
): 383-91
PMID26032551
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Metabolism has been a heavily investigated topic in cancer research for the past
decade. Although the role of aerobic glycolysis (the Warburg effect) in cancer
has been extensively studied, abnormalities in other metabolic pathways are only
just being understood in cancer. One such pathway is glycogen metabolism; its
involvement in cancer development, particularly in urothelial malignancies, and
possible ways of exploiting aberrations in this process for treatment are
currently being studied. New research shows that the glycogen debranching enzyme
amylo-?-1,6-glucosidase, 4-?-glucanotransferase (AGL) is a novel tumour
suppressor in bladder cancer. Loss of AGL leads to rapid proliferation of bladder
cancer cells. Another enzyme involved in glycogen debranching, glycogen
phosphorylase, has been shown to be a tumour promoter in cancer, including in
prostate cancer. Studies demonstrate that bladder cancer cells in which AGL
expression is lost are more metabolically active than cells with intact AGL
expression, and these cells are more sensitive to inhibition of both glycolysis
and glycine synthesis--two targetable pathways. As a tumour promoter and enzyme,
glycogen phosphorylase can be directly targeted, and preclinical inhibitor
studies are promising. However, few of these glycogen phosphorylase inhibitors
have been tested for cancer treatment in the clinical setting. Several possible
limitations to the targeting of AGL and glycogen phosphorylase might also exist.
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